A growing body of evidence suggests that a relatively rare subset of cells within a cancer subverts properties normally ascribed to stem cells in regenerating tissues, such as enhanced self-renewal and survival capacity. Recent studies suggest that these cancer stem cells (CSC) are resistant to treatments that target rapidly dividing cells. Recent studies suggest that in blast crisis chronic myeloid leukemia (BC CML) and some forms of acute myeloid leukemia (AML) CSC originate from the CD34+CD38+lineage− compartment of hematopoietic cells and can serially transplant blast crisis leukemia in immunodeficient mice.
Unlike stem cells in regenerating tissues, which are characterized by enhanced self-renewal and survival capacity, recent studies suggests that cancer stem cells (CSC) are resistant to treatments that target rapidly dividing cells.
With progression to blast crisis, CML stem cells become more resistant to therapies targeting BCR-ABL. As BCR-ABL targeted therapy initiates apoptosis, these results suggest that CML CSC may become increasingly resistant to apoptosis with progression.
Existing methods for predicting leukemia progression and drug susceptibility analyze the bulk of cells from a leukemia and do not quantitate Bcl-2 family molecules. However, not all cells in a leukemia are equivalent and CSCs in particular display aberrant expression of Bcl-2 molecules. Because CSCs drive the progression of leukemia, analysis and characterization of that population specifically could allow for better prediction of the course of the disease.